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. 2023 Apr 4;14:1638. doi: 10.1038/s41467-023-37269-3

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — Although SARS-CoV-2 is a respiratory virus, multiomics analysis demonstrates systemic changes related to inflammation and the hepatic acute phase response. In adults, the lung-liver axis alterations associated with COVID-19 lead to hypercoagulability and alterations in hemodynamics. As demonstrated in our microfluidics assays, pathologically elevated fibrinogen causes RBC aggregation that damages the endothelial glycocalyx, resulting in endotheliopathy and increased potential for microvascular thrombi formation. This appears to be a distinct mechanism in patients with COVID-19 when compared with patients with sepsis from other infectious causes. In contrast, analysis of samples from pediatric patients suggests that alterations in inflammatory signals cause immune dysregulation. MIS-C demonstrates greater immune dysregulation than acute pediatric COVID and results in a hyper-inflamed state, with an uncertain contribution of fibrinogen in mediating the vasculopathy observed clinically in MIS-C.